In a systematic review and meta-analysis of data from individual patients, we established a comprehensive set of LSM ranges, measured by TE in large cohorts of healthy individuals and persons susceptible to hepatic fibrosis. Regression analyses identified factors associated with LSMs made by TE with the medium and extra-large probes.

Mutations in hemochromatosis protein (HFE) or transferrin receptor 2 (TFR2) cause hereditary hemochromatosis (HH) by impeding production of the liver iron-regulatory hormone, hepcidin (HAMP). This study examined the effects of disruption of Hfe or Tfr2, either alone or together, on liver iron loading and injury in mouse models of HH. Iron status was determined in Hfe knockout (Hfe 2/2 ), Tfr2 Y245X mutant (Tfr2 mut ), and doublemutant (Hfe 2/2 3Tfr2 mut ) mice by measuring plasma and liver iron levels. Plasma alanine transaminase (ALT) activity, liver histology, and collagen deposition were evaluated to assess liver injury. Hepatic oxidative stress was assessed by measuring superoxide dismutase (SOD) activity and F 2 -isoprostane levels. Gene expression was measured by real-time polymerase chain reaction. Hfe 2/2 3Tfr2 mut mice had elevated hepatic iron with a periportal distribution and increased plasma iron, transferrin saturation, and non-transferrin-bound iron, compared with Hfe 2/2 , Tfr2 mut , and wild-type (WT) mice. Hamp1 expression was reduced to 40% (Hfe 2/2 and Tfr2 mut ) and 1% (Hfe 2/2 3Tfr2 mut ) of WT values. Hfe 2/2 3Tfr2 mut mice had elevated plasma ALT activity and mild hepatic inflammation with scattered aggregates of infiltrating inflammatory cluster of differentiation 45 (CD45)-positive cells. Increased hepatic hydoxyproline levels as well as Sirius red and Masson's Trichrome staining demonstrated advanced portal collagen deposition. Hfe 2/2 and Tfr2 mut mice had less hepatic inflammation and collagen deposition. Liver F 2 -isoprostane levels were elevated, and copper/zinc and manganese SOD activities decreased in Hfe 2/2 3Tfr2 mut , Tfr2 mut , and Hfe 2/2 mice, compared with WT mice. Conclusion: Disruption of both Hfe and Tfr2 caused more severe hepatic iron overload with more advanced lipid peroxidation, inflammation, and portal fibrosis than was observed with the disruption of either gene alone. The Hfe 2/2 3Tfr2 mut mouse model of iron-induced liver injury reflects the liver injury phenotype observed in human HH. (HEPATOLOGY 2012;56:585-593)

No abstract

Our results suggest that a combination of MRI measures, that include selected texture features from T2 -weighted images, may be a useful tool for excluding fibrosis in patients with liver disease. However, texture analysis of MRI performs only modestly when applied to the classification of patients in the mild and intermediate fibrosis stages.